Proteomic analysis in hidradenitis suppurativa reveals systemic inflammation in all disease stages

Hidradenitis suppurativa (HS) is a chronic inflammatory skin disease characterized by painful, inflamed lesions in the apocrine gland-bearing regions and systemic involvement. While inflammatory cytokines including IL-6 and IL-17A have been implicated in HS pathogenesis, the extent and clinical correlates of systemic inflammation remain incompletely defined.

To characterize systemic inflammatory profiles in a well-defined cohort of largely untreated HS patients and assess associations with disease severity and duration, quality of life and lifestyle factors.

In this case-control, single-centre study, serum samples were collected from 44 patients with HS and 44 age- and sex-matched healthy controls, and 92 immune-related proteins were quantified by the Olink® Target 96 Inflammation panel. Clinical parameters included age, sex, BMI, smoking status, Hurley stage, International Hidradenitis Suppurativa Severity Score System (IHS4), disease duration and Dermatology Life Quality Index (DLQI). Associations were evaluated by Spearman's correlations and Mann-Whitney U tests.

Thirty-seven inflammatory proteins were significantly different between HS patients and controls. The most significantly increased mediators included TGF-α, IL-6, OSM, IL-8/CXCL8, HGF, VEGFA and IL-17A. Notably, several mediators, such as TGF-α, OSM, IL-8/CXCL8, IL-7, TNFSF14 and HGF, were elevated already in mild HS. IL-6, IL-17A, CCL19, VEGFA, CCL20 increased progressively with increasing Hurley stage. IL-6 and HGF levels showed positive correlations with IHS4 and DLQI scores, while IL-17A and CCL19 were associated with longer disease duration.

Our exploratory proteomic analysis reveals systemic inflammation across all stages of HS, including early disease. IL-6 and HGF were associated with severity and quality of life impairment, whereas IL-17A and CCL19 may reflect disease chronicity. Although the relatively small cohort and potential confounding warrant cautious interpretation, these findings reinforce the concept of HS as a systemic inflammatory disorder and support early, comprehensive management to mitigate long-term burden and comorbidities.